VPA-985 selectively blocks the renal receptor of vasopressin and thereby allows excretion of free water which may be efficacious in the treatment of hyponatremia. Experimental preclinical and clinical evidence demonstrates that VPA-985 is an orally active, competitive, nonpeptide vasopressin receptor antagonist. Its primary site of action is the V2 receptor located on the renal medullary collecting duct where it inhibits water reabsorption. Oral doses appear to be rapidly absorbed with dose-related increases in the drug's maximum plasma concentration (Cmax) and the area under the curve (AUC). VPA-985 produces dose-related increases in urine flow and free water clearance with prolongation of effect at higher doses and corresponding increases in serum sodium and serum osmolality and decreases in urine osmolality. Clinical data available demonstrate that VPA-985 is an effective aquaretic agent that is likely to have therapeutic utility in the treatment of diseases associate with water accumulation and hyponatremia.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
3M01RR000052-38S2
Application #
6264072
Study Section
Project Start
1998-12-01
Project End
1999-11-30
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
38
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Johns Hopkins University
Department
Type
DUNS #
045911138
City
Baltimore
State
MD
Country
United States
Zip Code
21218
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